Authors

Bo Liu1*, Yueqiu Gao2, Yanming Zheng1, Xiaomin Wang1, Jiufei Wang1


Departments

1Department of Neurosurgery, Daqing Oilfield General Hospital, Daqing 163411, Heilongjiang, China - 2Department of Gastroenterology and Hepatology, the Fifth Affiliated Hospital of Harbin Medical University, Daqing 163316, Heilongjiang, China

Abstract

Objective: To analyze the protective effect of gallocatechin gallate (EGCG) on neuronal cell activity injury and oxidative damage induced by rotenone. 

Methods: Human neuroblastoma cells SH-SY5Y cultured with rotenone were used to model Parkinson’s disease cells in vitro, and then treated with EGCG 0,10,20,40µmol/L and a positive drug (pilagilan, 50µmol/L) respectively. The CCK-8 method was used to detect the survival rate of nerve cells in each group, while the Western blot method was used to detect protein (Bax, TH, Nrf2) expression in nerve cells and the content of oxidative damage factors in each group. 

Results: The survival rate of nerve cells in the EGCG and positive control groups was significantly higher than that in the model control group (P<0.05). The expression of Bax protein in the EGCG 20,40µmol/L dose group and in the positive control group was significantly lower than that in the model control group (P<0.05). The expression of TH protein in the EGCG 10, 20µmol/L dose group and in the positive control group was significantly higher than that in the model group (P<0.05). The Nrf2 protein of nerve cells in the EGCG treatment group and in the positive control group was significantly higher than that in the model group (P<0.05). 

Conclusions: EGCG seems to protect against neuronal cell damage and oxidative damage caused by rotenone through antioxidant stress injury, and this mechanism may be related to the signaling pathway by which EGCG promotes the activation of Nrf2/ARE protein expression. 

Keywords

EGCG, rotenone, parkinson's disease, nerve cell, oxidative damage, protective effect.

DOI:

10.19193/0393-6384_2022_1_34